ArticleBioMed research international2013
Interleukin-33 drives activation of alveolar macrophages and airway inflammation in a mouse model of acute exacerbation of chronic asthma.
Article in BioMed research international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 31 citations in OpenAlex.
- Transient lung eosinophilia during breakthrough influenza infection in vaccinated mice is associated with protective and balanced Type 1/2 immune responses.Journal of virology · 2025Article
- TNFR2 Signaling Enhances ILC2 Survival, Function, and Induction of Airway Hyperreactivity.Cell reports · 2019Article
- Sex differences in the inflammatory immune response to multi-walled carbon nanotubes and crystalline silica.Inhalation toxicology · 2019Article
- IL-33 delivery induces serous cavity macrophage proliferation independent of interleukin-4 receptor alpha.European journal of immunology · 2016Article
- IL-33 Contributes to Schistosoma japonicum-induced Hepatic Pathology through Induction of M2 Macrophages.Scientific reports · 2016Article
- The IL-33 receptor (ST2) regulates early IL-13 production in fungus-induced allergic airway inflammation.Mucosal immunology · 2016Article
- Rhinoviral stimuli, epithelial factors and ATP signalling contribute to bronchial smooth muscle production of IL-33.Journal of translational medicine · 2015Article
- Response of airway epithelial cells to double-stranded RNA in an allergic environment.Translational respiratory medicine · 2014Article
- Key mediators in the immunopathogenesis of allergic asthma.International immunopharmacology · 2014Review
- Respiratory viral infection, epithelial cytokines, and innate lymphoid cells in asthma exacerbations.Journal of leukocyte biology · 2014Review
- Ambient particulate matter induces an exacerbation of airway inflammation in experimental asthma: role of interleukin-33.Clinical and experimental immunology · 2014Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the role of interleukin-33 (IL-33) in airway inflammation in an experimental model of an acute exacerbation of chronic asthma, which reproduces many of the features of the human disease. Systemically sensitized female BALB/c mice were challenged with a low mass concentration of aerosolized ovalbumin for 4 weeks to induce chronic asthmatic inflammation and then received a single moderate-level challenge to trigger acute airway inflammation simulating an asthmatic exacerbation. The inflammatory response and expression of cytokines and activation markers by alveolar macrophages (AM) were assessed, as was the effect of pretreatment with a neutralizing antibody to IL-33. Compared to chronically challenged mice, AM from an acute exacerbation exhibited significantly enhanced expression of markers of alternative activation, together with enhanced expression of proinflammatory cytokines and of cell surface proteins associated with antigen presentation. In parallel, there was markedly increased expression of both mRNA and immunoreactivity for IL-33 in the airways. Neutralization of IL-33 significantly decreased both airway inflammation and the expression of proinflammatory cytokines by AM. Collectively, these data indicate that in this model of an acute exacerbation of chronic asthma, IL-33 drives activation of AM and has an important role in the pathogenesis of airway inflammation.
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